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Surgical Anaesthesia Powder Levobupivacaine For Pain Killer CAS NO:27262-47-1
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Density:1.0 0.1 g/cm3
Boiling Point:423.4 45.0 C at 760 mmHg
Melting Point:254C (dec.)(lit.)
Flash Point:209.9/28.7 C
The bupivacaine molecule is a racemic compound.Levobupivacaine is the S-enantiomer of bupivacaine and is thought to have less cardiotoxic potential than the R-enantiomer.The pharmacokinetic parameters of levobupivacaine are similar to those of bupivacaine.
Levobupivacaine has been studied in surgical anaesthesia and for pain management.It can be used for local infiltration,epidural,intrathecal and peripheral nerve blocks.For epidural analgesia it can be given with clonidine.Double-blind comparisons of levobupivacaine and bupivacaine show that their anaesthetic effects are similar.
Levobupivacaine (rINN) is a local anaesthetic drug belonging to the amino amide group. It is the S-enantiomer of bupivacaine.
The hydrochloride salt of levobupivacaine, an amide derivative with anesthetic property. Levobupivacaine reversibly binds voltage-gated sodium channels to modulate ionic flux and prevent the initiation and transmission of nerve impulses (stabilizing neuronal membrane), thereby resulting in analgesia and anesthesia. In comparison with racemic bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action.
Levobupivacaine is an amide-type local anaesthetic. Levobupivacaine acts via blockade of voltage-sensitive ion channels in neuronal membranes, preventing transmission of nerve impulses. Localised and reversible anaesthesia is produced by interference with the opening of the sodium channel, which inhibits conduction of the action potential in nerves involved in sensory and motor activity and sympathetic activity.  Levobupivacaine displaces 3H-BTX from sodium channels of rat brain synaptosomes with IC50 of 2.9 μM and Hill coefficients of 1.2. When cell membrane is held at -80 mV, -70 mV, -60 mV or -100 mV, Levobupivacaine shows tonic inhibition of sodium channel in GH3 cells with IC50s of 132.1, 37.6, 21.6 and 264 μM, respectively.  Levobupivacaine depresses action potential of isolated axon in vitro. Levobupivacaine (1mM) depresses action potential amplitude and maximal rate of rise of action potential (dV/dtmax) in the crayfish giant axons with value of 88 and 81 respectively, after perfusion for 15 min.  Levobupivacaine also displays activity on cardiac ion channels. In isolated ventricular myocytes, the apparent affinity for inactivated state of the sodium channel is 4.8 μM for Levobupivacaine, with a calculated KD of 39μM. On inhibition of cardiac delayed rectifier potassium channels (hKv1.5), the steady-state block for Levobupivacaine (20 μM) is 31%, with a calculated KD of 27.3 μM. Levobupivacaine may also inhibit cardiac calcium channels. 10 μM Levobupivacaine produces a 50% decrease in contractile force of guinea-pig papillary muscles.
Compared to bupivacaine, levobupivacaine is associated with less vasodilation and has a longer duration of action. It is approximately 13 percent less potent (by molarity) than racemic bupivacaine and has a longer motor block onset time.
Levobupivacaine is indicated for local anaesthesia including infiltration, nerve block, ophthalmic, epidural and intrathecal anaesthesia in adults; and infiltration analgesia in children.
Levobupivacaine is contraindicated for IV regional anaesthesia (IVRA).
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